Schizophrenia, brain inflammation and depression

Schizophrenia shares underlying causal mechanisms with depression that are important for case management and treatment. A paper just published in the journal Progress in Neuro-Psychopharmacology and Biological Psychiatry highlights key features of the inflammatory process in schizophrenia that clinicians should be aware of. The authors state:

"Schizophrenia and depression are two common and debilitating psychiatric conditions. Up to 61% of schizophrenic patients have comorbid clinical depression, often undiagnosed. Both share significant overlaps in underlying biological processes, which are relevant to the course and treatment of both conditions."

All of these processes in both schizophrenia and depression are linked in some way to inflammation:

"Shared processes include changes in cell‐mediated immune and inflammatory pathways, e.g. increased levels of pro-inflammatory cytokines and a Th1 response; activation of oxidative and nitrosative stress (O&NS) pathways, e.g. increased lipid peroxidation, damage to proteins and DNA; decreased antioxidant levels, e.g. lowered coenzyme Q10, vitamin E, glutathione and melatonin levels; autoimmune responses; and activation of the tryptophan catabolite (TRYCAT) pathway through induction of indoleamine-2,3-dioxygenase. Both show cognitive and neurostructural evidence of a neuroprogressive process."

The authors assert that patients with schizophrenia are immunologically predisposed to depression:

"Here we review the interlinked nature of these biological processes, suggesting that schizophrenia is immunologically primed for an increased expression of depression. Such a conceptualization explains, and incorporates, many of the current perspectives on the nature of schizophrenia and depression, and has implications for the nature of classification and treatment of both disorders."

As readers here likely know, latent autoimmune phenomena are often triggered by infection. The authors discuss how this comes into play in promoting and differentiating schizophrenia and depression in regard to maternal infections.

"An early developmental etiology to schizophrenia, driven by maternal infection, with subsequent impact on offspring immuno-inflammatory responses, creates alterations in the immune pathways, which although priming for depression, also differentiates the two disorders."

For concerned clinicians this offers a rich assortment of pathways that can be investigated with appropriate tests as candidates for interventional support.Relevant to this topic is a presentation on psychiatric conditions as immune disorders entitled Redefining Psychiatric and Neurologic Co-morbidities as Systemic Dysfunction delivered at the Autoimmunity Congress Asia in Singapore last September by Dr Roswitha Goetze-Pelka of the Ev. Krankenhaus Bethanien in Greifswald, Germany: